Unintended Inhalation of Nitric Oxide by Contamination of Compressed Air: Physiologic Effects and Interference with Intended Nitric Oxide Inhalation in Acute Lung Injury

Background: Compressed air from a hospital's central gas supply may contain nitric oxide as a result of air pollution. Inhaled nitric oxide may increase arterial oxygen tension and decrease pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. Therefore, the authors wanted to determine whether unintentional nitric oxide inhalation by contamination of compressed air influences arterial oxygen tension and pulmonary vascular resistance and interferes with the therapeutic use of nitric oxide.

Methods: Nitric oxide concentrations in the compressed air of a university hospital were measured continuously by chemiluminescence during two periods (4 and 2 weeks). The effects of unintended nitric oxide inhalation on arterial oxygen tension (n = 15) and on pulmonary vascular resistance (n = 9) were measured in patients with acute lung injury and acute respiratory distress syndrome by changing the source of compressed air of the ventilator from the hospital's central gas supply to a nitric oxide-free gas tank containing compressed air. In five of these patients, the effects of an additional inhalation of 5 ppm nitric oxide were evaluated.

Results: During working days, compressed air of the hospital's central gas supply contained clinically effective nitric oxide concentrations (> 80 parts per billion) during 40% of the time. Change to gas tank-supplied nitric oxide-free compressed air decreased the arterial oxygen tension by 10% and increased pulmonary vascular resistance by 13%. The addition of 5 ppm nitric oxide had a minimal effect on arterial oxygen tension and pulmonary vascular resistance when added to hospital-supplied compressed air but improved both when added to tank-supplied compressed air.     

Brief Periods of Nitric Oxide Inhalation Protect against Myocardial Ischemia-Reperfusion Injury

Background: Prolonged breathing of nitric oxide reduces myocardial ischemia-reperfusion injury, but the precise mechanisms responsible for the cardioprotective effects of inhaled nitric oxide are incompletely understood.

Methods: The authors investigated the fate of inhaled nitric oxide (80 parts per million) in mice and quantified the formation of nitric oxide metabolites in blood and tissues. The authors tested whether the accumulation of nitric oxide metabolites correlated with the ability of inhaled nitric oxide to protect against cardiac ischemia-reperfusion injury.

Results: Mice absorbed nitric oxide in a nearly linear fashion (0.19 +/- 0.02 [mu]mol/g [middle dot] h). Breathing nitric oxide rapidly increased a broad spectrum of nitric oxide metabolites. Levels of erythrocytic S-nitrosothiols, N-nitrosamines, and nitrosyl-hemes increased dramatically within 30 s of commencing nitric oxide inhalation. Marked increases of lung S-nitrosothiol and liver N-nitrosamine levels were measured, as well as elevated cardiac and brain nitric oxide metabolite levels. Breathing low oxygen concentrations potentiated the ability of inhaled nitric oxide to increase cardiac nitric oxide metabolite levels. Concentrations of each nitric oxide metabolite, except nitrate, rapidly reached a plateau and were similar after 5 and 60 min. In a murine cardiac ischemia-reperfusion injury model, breathing nitric oxide for either 5 or 60 min before reperfusion decreased myocardial infarction size as a fraction of myocardial area at risk by 31% or 32%, respectively.     

Rebound Pulmonary Hypertension After Inhalation of Nitric Oxide

Background. We describe the hemodynamic response to initiation and withdrawal of inhaled nitric oxide (NO) in infants with pulmonary hypertension after surgical repair of total anomalous pulmonary venous connection.

Methods. Between January 1, 1992, and January 1, 1995, 20 patients underwent repair of total anomalous pulmonary venous connection. Nine patients had postoperative pulmonary hypertension and received a 15-minute trial of inhaled NO at 80 parts per million. Five of these patients received prolonged treatment with NO at 20 parts per million or less.

Results. Mean pulmonary artery pressure decreased from 35.6 ± 2.4 to 23.7 ± 2.0 mm Hg (mean ± standard error of the mean) (p = 0.008), and pulmonary vascular resistance decreased from 11.5 ± 2.0 to 6.4 ± 1.0 U · m² (p = 0.03). After prolonged treatment with NO, pulmonary artery pressure increased transiently in all patients when NO was discontinued.

Conclusions. After operative repair of total anomalous pulmonary venous connection, inhaled NO selectively vasodilated all patients with pulmonary hypertension. Withdrawal of NO after prolonged inhalation was associated with transient rebound pulmonary hypertension that dissipated within 60 minutes. Appreciation of rebound pulmonary hypertension may have important implications for patients with pulmonary hypertensive disorders when interruption of NO inhalation is necessary or when withdrawal of NO is planned.     

iNOS及eNOS mRNA表达在急性坏死性胰腺炎肺损伤中的作用

目的通过观察急性坏死性胰腺炎(acute necrotizing pancreatitis,ANP)大鼠肺组织中诱导型一氧化氮合酶(inducible nitric oxide synthase,i NOS)mRNA和内皮型一氧化氮合酶(endothelial nitric oxide synthase,eNOS)mRNA的表达,探讨内源性NOS在ANP肺损伤中的作用。方法 40只Wistar大鼠随机分为ANP组(n=30)和假手术组(SO组,n=10),采用5%牛磺胆酸钠逆行胆胰管注射法建立大鼠ANP模型。光镜下观察ANP造模后3 h、6 h及12 h时大鼠肺组织病理变化,并应用RT-PCR法检测相应时相肺组织中i NOS及eNOS mRNA的表达水平。结果随着病程延长,ANP组肺组织可见不同程度的充血、水肿、炎性细胞浸润、出血、坏死等病理损害,各时间点其肺损伤评分均明显高于SO组(P0.05),且呈逐渐升高趋势(P0.05)。ANP组3 h、6 h及12 hi NOS和eNOS mRNA的表达水平较SO组均有明显升高(P0.05)。结论肺组织中i NOS及eNOS mRNA的过度表达可能是大鼠ANP肺损伤发生的重要原因之一,这为采用抑制i NOS及eNOS mRNA的表达减轻ANP肺损伤的治疗手段提供了理论依据。     

Nitric Oxide Produced by Inducible Nitric Oxide Synthase Delays Gastric Emptying in Lipopolysaccharide-treated Rats

Background: Endotoxin induces nitric oxide synthase (NOS), resulting in relaxation of gastric smooth muscle. The authors examined the effect of NO produced in response to lipopolysaccharide (LPS) treatment on gastric emptying in rats, and they also examined the effects of a selective inhibitor of inducible NOS (iNOS), aminoguanidine, and a suppressor of iNOS gene expression, dexamethasone.

Methods: Male Wistar rats weighing 200-250 g were used. LPS-treated rats received LPS (0.2-10 mg/kg) diluted in physiologic saline intraperitoneally. Before and at different intervals up to 8 h after administration of LPS, measurements of gastric emptying were performed in groups of 3-5 rats, by determining the amount of phenol red remaining in the stomach 20 min after intragastric instillation. In additional group of LPS (2 mg/kg)-treated rats, the gastric fundus was isolated 6 h after administration, and the tension changes in response to L-arginine, a substrate for NOS, and electrical transmural stimulation (3 Hz, 5 s) were recorded isometrically.

Results: (1) Gastric emptying was delayed by pretreatment with LPS in a dose- and time-dependent fashion (reduction from 68 +/- 12% to 22 +/- 7% with a dose of 2 mg/kg for 6 h). Aminoguanidine (50 mg/kg) or dexamethasone (5 mg/kg) partially inhibited the delay (to 39 +/- 4% or to 40 +/- 10%, respectively). (2) L-arginine (0.1 mM) produced a relaxation (28 +/- 2% reduction in active tension) in the gastric fundus strips isolated from LPS-treated rats but not from LPS-untreated rats. The relaxation was inhibited by aminoguanidine (1 mM). In contrast, the relaxation response to the electrical stimulation was not affected by aminoguanidine (0.1-1 mM).     

Factors Influencing the Tracheal Fluctuation of Inhaled Nitric Oxide in Patients with Acute Lung Injury

Background: Inhaled nitric oxide (NO) improves arterial oxygenation in patients with acute lung injury (ALI) by selectively dilating pulmonary vessels perfusing ventilated lung areas. It can be hypothesized that NO uptake from the lung decreases with increasing ventilation perfusion mismatch. This study was undertaken to determine the factors influencing the fluctuation of tracheal NO concentration over the respiratory cycle as an index of NO pulmonary uptake in patients with ALI.

Methods: By using a prototype system (Opti-NO) delivering a constant flow of NO only during the inspiratory phase, 3 and 6 ppm of NO were administered during controlled mechanical ventilation into a lung model and to 11 patients with ALI. All patients had a thoracic computed tomography (CT) scan. Based on an analysis of tomographic densities, lungs were divided into three zones: normally aerated (-1.000 to 500 Hounsfield units [HU]), poorly aerated (-500 to -100 HU), and nonaerated (-100 to +100 HU), and the volume of each zone was computed. Concentrations of NO in the inspiratory limb and trachea were continuously measured by a fast-response chemiluminescence apparatus.

Results: In the lung model, tracheal NO concentration was stable with minor fluctuation. In contrast, in patients, tracheal NO concentration fluctuated widely during the respiratory cycle (55 +/- 10%). Because uptake of NO from the lungs was absent in the lung model but present in the patients, this fluctuation was considered as an index of pulmonary uptake of NO. This was further substantiated by (1) the coincidence of the peak and minimum tracheal NO concentration with the end-inspiratory and end-expiratory phases, respectively, and (2) continued decrease of tracheal NO concentration during prolonged expiratory phase. In patients with ALI, the fluctuation of tracheal NO concentration expressed as the difference between inspiratory and expiratory NO concentrations divided by inspiratory NO concentration was greater at 6 ppm than at 3 ppm (P < 0.01), was linearly correlated with normally aerated lung volume, inversely correlated with alveolar dead space and with poorly aerated lung volume.     

Pulmonary Vasoconstriction during Regional Nitric Oxide Inhalation: Evidence of a Blood-borne Regulator of Nitric Oxide Synthase Activity

Background: Inhaled nitric oxide (INO) is thought to cause selective pulmonary vasodilation of ventilated areas. The authors previously showed that INO to a hyperoxic lung increases the perfusion to this lung by redistribution of blood flow, but only if the opposite lung is hypoxic, indicating a more complex mechanism of action for NO. The authors hypothesized that regional hypoxia increases NO production and that INO to hyperoxic lung regions (HL) can inhibit this production by distant effect.

Methods: Nitric oxide concentration was measured in exhaled air (NOE), NO synthase (NOS) activity in lung tissue, and regional pulmonary blood flow in anesthetized pigs with regional left lower lobar (LLL) hypoxia (fraction of inspired oxygen [Fio2] = 0.05), with and without INO to HL (Fio2 = 0.8), and during cross-circulation of blood from pigs with and without INO.

Results: Left lower lobar hypoxia increased exhaled NO from the LLL (NOELLL) from a mean (SD) of 1.3 (0.6) to 2.2 (0.9) parts per billion (ppb) (P < 0.001), and Ca2+-dependent NOS activity was higher in hypoxic than in hyperoxic lung tissue (197 [86]vs. 162 [96] pmol [middle dot] g-1 [middle dot] min-1, P < 0.05). INO to HL decreased the Ca2+-dependent NOS activity in hypoxic tissue to 49 [56] pmol [middle dot] g-1 [middle dot] min-1 (P < 0.01), and NOELLL to 2.0 [0.8] ppb (P < 0.05). When open-chest pigs with LLL hypoxia received blood from closed-chest pigs with INO, NOELLL decreased from 2.0 (0.6) to 1.5 (0.4) ppb (P < 0.001), and the Ca2+-dependent NOS activity in hypoxic tissue decreased from 152 (55) to 98 (34) pmol [middle dot] g-1 [middle dot] min-1 (P = 0.07). Pulmonary vascular resistance increased by 32 (21)% (P < 0.05), but more so in hypoxic (P < 0.01) than in hyperoxic (P < 0.05) lung regions, resulting in a further redistribution (P < 0.05) of pulmonary blood flow away from hypoxic to hyperoxic lung regions.     

Statistical Prediction of the Type of Gastric Aspiration Lung Injury Based on Early Cytokine/Chemokine Profiles

Background: Unwitnessed gastric aspiration can be a diagnostic dilemma, and early discrimination of different forms may help to identify individuals with increased risk of development of severe clinical acute lung injury or acute respiratory distress syndrome. The authors hypothesized that inflammatory mediator profiles could be used to help diagnose different types of gastric aspiration.

Methods: Diagnostic modeling using a newly modified receiver operator characteristic approach was applied to recently published data from our laboratory on lavaged inflammatory mediators from rodents given intratracheal normal saline, hydrochloric acid, small nonacidified gastric particles, or a combination of acid and small gastric particles. Multiple animal groups and postaspiration times of injury were analyzed to gauge the applicability of the predictive approach: rats (6 and 24 h), C57/BL6 wild-type mice (5 and 24 h), and transgenic mice on the same background deficient in the gene for monocyte chemoattractant protein 1 (MCP-1 [-/-] mice; 5 and 24 h).

Results: Overall, the four types of aspiration were correctly discriminated in 85 of 96 rats (89%), 72 of 78 wild-type mice (92%), and 59 of 73 MCP-1 (-/-) mice (81%) by models that used a maximum of only two mediators. The severe "two-hit" aspirate of the combination of acid and small gastric particles was correctly predicted in 21 of 24 rats, 23 of 23 wild-type mice, and 21 of 21 MCP-1 (-/-) mice. Specific best-fit mediators or mediator pairs varied with aspirate type, animal type, and time of injury. Cytokines and chemokines that best predicted the combination of acid and small gastric particles were cytokine-induced neutrophil chemoattractant 1 (6 h) and MCP-1 (24 h) in rats, tumor necrosis factor [alpha]/macrophage inflammatory protein 2 (5 h) and tumor necrosis factor [alpha]/MCP-1 (24 h) in wild-type mice, and tumor necrosis factor [alpha]/macrophage inflammatory protein 2 (5 h) and tumor necrosis factor [alpha]/keratinocyte-derived cytokine (24 h) in MCP-1 (-/-) mice.     

Effects of Inhaled Nitric Oxide Following Lung Transplantation

Abstract Background: Lung transplantation offers an established therapeutic option for end‐stage lung disease. It is associated with several complications, and early allograft failure is one of the most devastating among all. Different studies are focused on an attempt to minimize these complications, especially transplant failure. We aimed to evaluate the effects of inhaled nitric oxide (iNO) treatment in patients receiving lung transplantation. Methods: Nine patients (six female, three male; mean age 42.9 ± 15.8) requiring lung transplantation for end‐stage pulmonary disease—chronic obstructive pulmonary disease (three patients), cystic fibrosis (three patients), scleroderma and systemic sclerosis (two patients), Eisenmenger's syndrome (one patient), and treated with iNO were included in this retrospective study. Hemodynamic data (mean arterial pressure, mean pulmonary arterial pressure, heart rate) and respiratory parameters were analyzed. Pretreatment data were compared with the post‐iNO treatment data at 6–8 hours and 12–14 hours. Results: The inhalation of nitric oxide was started with an initial dose of 40 parts per million (ppm) and the dose was gradually decreased until hemodynamic and pulmonary stability was achieved. Six patients underwent double‐lung transplantation and three single‐lung transplantations were performed. Cardiopulmonary bypass was used in seven patients. The iNO therapy was started before transplantation in five patients, after the procedure in four patients. Mean iNO therapy duration was 83.2 ± 74.4 hours. The administration of iNO resulted in a significant reduction in mean pulmonary arterial pressure (36.8 ± 15.8 mm Hg to 22 ± 6.8 mm Hg at 6–8 hours and 22.8 ± 7.96 mm Hg at 12–14 hours). Mean systemic arterial pressure slightly increased at 6–8 hours and significantly increased at 12–14 hours (70.2 ± 6.3 mm Hg to 90.1 ± 11.96 mm Hg). Heart rate was not significantly affected with the treatment. Arterial oxygenation improved with the treatment. All patients except one showed improvement of overall respiratory functions. The mean duration of mechanical ventilation was 12.8 ± 10.9 days. Mortality occurred in one patient due to neurologic injury. NO₂ and methemoglobin levels were closely monitored during the treatment. Methemoglobinemia did not occur and NO₂ levels remained between 0.1 and 0.4 ppm. Conclusion: Nitric oxide inhalation for the prevention and treatment of early allograft failure in lung transplant recipients is encouraging. It is superior to other vasodilators with its selectivity to the pulmonary vasculature, while having no significant side effects on systemic circulation. It appears to improve gas exchange and oxygenation properties. Further prospective randomized studies will aid to standardize inhalation nitric oxide therapy.     

Nitric Oxide and the Lung: An Overview

Abstract: This brief discussion focuses on the effects of nitric oxide (NO) in the lung. A short introduction of some of the physical characteristics of the NO gas molecule and the endogenous production of NO by the vascular endothelium is addressed first. This is followed by a review of inhaled NO use as a hronchodilator of the airway and recent findings of the endogenous production of NO during positive end-expiratory pressure and the possible role of NO produced in the paranasal Sinuses. Next, the use of inhaled NO for both pulmonary hypertension and improvement in oxygenation under a variety of clinical situations is discussed. Finally, some suggestions are given regarding the safe delivery of inhaled NO during clinical applications using a facemask, an anesthesia circuit, and a mechanical ventilator.     

川芎嗪对兔胃液吸入性肺损伤中白细胞介素-8的影响

目的:探讨白细胞介素-8(IL-8)在兔胃液吸入性肺损伤中的变化及川芎嗪(Ligustrazini,Lig)的保护作用和机制。方法:通过兔气管内注入胃液的方法复制误吸性肺损伤动物模型,并以Lig为干预因素,侧重观察在其急性发病过程中支气管肺泡灌洗液(BALF)中IL-8的变化。结果:胃液误吸后BALF中IL-8含量升高,Lig治疗后IL-8显著降低。结论:Lig通过拮抗IL-8的产生,有效地减轻了由胃液误吸引起的急性肺损伤。     

大鼠脊髓损伤后诱导型一氧化氮合酶基因表达变化的实验研究

目的探讨大鼠脊髓损伤后诱导型一氧化氮合酶(iNOS)mRNA表达的变化规律.方法SD大鼠48只,随机分为8组,采用Allen's脊髓损伤打击模型,以逆转录-聚合酶链反应(RT-PCR)法测定伤段脊髓组织iNOS mRNA表达情况.结果iNOS mRNA在脊髓损伤前即有表达,损伤后早期无明显变化,伤后72h开始升高,1周时达到高峰.结论脊髓继发性损害的持续时间可能大于传统观念,针对继发性损害所作的治疗应持续至脊髓损伤后较长的一段时间.     

Recurrent Aspiration Pneumonia after Laparoscopic Adjustable Gastric Banding

Laparoscopic adjustable gastric banding is a popular therapeutic option for morbid obesity. Band slippage, pouch enlargement and esophageal dilatation are occasional late complications of this procedure. There are rare reports of recurrent aspiration after banding. We report a 44-year-old female suffering from dysphagia and aspiration pneumonia 2 years after adjustable banding. Her esophagus was dilated to 6 cm, and videocinematography showed a severe achalasia-like disorder.Withdrawal of fluid from the band should be immediate, and relieved the stomal obstruction in this patient. Aspiration pneumonia is a serious late complication, which is easily treated by deflation of the band.     

Hypoxic Pulmonary Vasoconstriction in Nonventilated Lung Areas Contributes to Differences in Hemodynamic and Gas Exchange Responses to Inhalation of Nitric Oxide

Background: Enhancement of hypoxic pulmonary vasoconstriction (HPV) in nonventilated lung areas by almitrine increases the respiratory response to inhaled nitric oxide (NO) in patients with acute respiratory distress syndrome (ARDS). Therefore the authors hypothesized that inhibition of HPV in nonventilated lung areas decreases the respiratory effects of NO.

Methods: Eleven patients with severe ARDS treated by venovenous extracorporeal lung assist were studied. Patients' lungs were ventilated at a fraction of inspired oxygen (FIO2) of 1.0. By varying extracorporeal blood flow, mixed venous oxygen tension (PO2; partial oxygen pressure in mixed venous blood [Pv with barO2]) was adjusted randomly to four levels (means, 47, 54, 64 and 84 mmHg). Extracorporeal gas flow was adjusted to prevent changes in mixed venous carbon dioxide tension [Pv with barCO2]). Hemodynamic and gas exchange variables were measured at each level before, during, and after 15 ppm NO.

Results: Increasing Pv with barO2 from 47 to 84 mmHg resulted in a progressive decrease in lung perfusion pressure (PAP-PAWP; P < 0.05) and pulmonary vascular resistance index (PVRI; P < 0.05) and in an increase in intrapulmonary shunt (Q with dotS /Q with dotT; P < 0.05). Pv with barCO2 and cardiac index did not change. Whereas the NO-induced reduction in PAP-PAWP was smaller at high Pv with barO2, NO-induced decrease in Q with dotS /Q with dotT was independent of baseline Pv with barO2. In response to NO, arterial PO2 increased more and arterial oxygen saturation increased less at high compared with low Pv with barO2.     

Nitric Oxide Mechanism of Protection in Ischemia and Reperfusion Injury

In 1992 nitric oxide (NO) was declared molecule of the year by Science magazine, and ever since research on this molecule continues to increase. Following this award, NO was shown to be a mediator/protector of ischemia and reperfusion injury in many organs, such as the heart, liver, lungs, and kidneys. Controversy has existed concerning the actual protective effects of NO. However, literature from the past 15 years seems to reinforce the consensus that NO is indeed protective. Some of the protective actions of NO in ischemia and reperfusion are due to its potential as an antioxidant and anti-inflammatory agent, along with its beneficial effects on cell signaling and inhibition of nuclear proteins, such as NF-κ B and AP-1. New therapeutic potentials for this drug are also continuously emerging. Exogenous NO and endogenous NO may both play protective roles during ischemia and reperfusion injury. Sodium nitroprusside and nitroglycerin have been used clinically with much success; though only recently have they been tested and proven effective in attenuating some of the injuries associated with ischemia and reperfusion. NO inhalation has, in the past, mostly been used for its pulmonary effects, but has also recently been shown to be protective in other organs. The potential of NO in the treatment of ischemic disease is only just being realized. Elucidation of the mechanism by which NO exerts its protective effects needs further investigation. Therefore, this paper will focus on the mechanistic actions of NO in ischemia and reperfusion injury, along with the compound's potential therapeutic benefits.     

大鼠脊髓损伤后诱导型-氧化氮合酶基因表达变化的实验研究

目的 :探讨大鼠脊髓损伤后诱导型一氧化氮合酶 (iNOS)mRNA表达的变化规律。方法 :SD大鼠 48只 ,随机分为 8组 ,采用Allen’s脊髓损伤打击模型 ,以逆转录 -聚合酶链反应 (RT -PCR)法测定伤段脊髓组织iNOSmRNA表达情况。结果 :iNOSmRNA在脊髓损伤前即有表达 ,损伤后早期无明显变化 ,伤后 72h开始升高 ,1周时达到高峰。结论 :脊髓继发性损害的持续时间可能大于传统观念 ,针对继发性损害所作的治疗应持续至脊髓损伤后较长的一段时间     

Desflurane Increases Pulmonary Alveolar-Capillary Membrane Permeability after Aortic Occlusion-Reperfusion in Rabbits: Evidence of Oxidant-mediated Lung Injury

Background: Pulmonary injury occurs after vascular surgery, with xanthine oxidase (an oxidant generator) released from reperfusing liver and intestines mediating a significant component of this injury. Because halogenated anesthetics have been observed to enhance oxidant-mediated injury in vitro, the authors hypothesized that desflurane would increase alveolar-capillary membrane permeability mediated by circulating xanthine oxidase after thoracic occlusion and reperfusion.

Methods: Rabbits were assigned to one of five groups: aorta occlusion groups administered desflurane (n = 14), desflurane and tungstate (xanthine oxidase inactivator, n = 12), fentanyl plus droperidol (n = 13), and two sham-operated groups (desflurane, n = 7 and fentanyl plus droperidol, n = 7). Aortic occlusion was maintained for 45 min with a balloon catheter, followed by 3 h of reperfusion. Alveolar-capillary membrane permeability was assessed by measurement of bronchoalveolar lavage fluid protein. Xanthine oxidase activity was determined in plasma and lung tissue. Ascorbic acid content (an antioxidant) was determined in lung tissue.

Results: Desflurane was associated with significantly increased alveolar-capillary membrane permeability after aortic occlusion-reperfusion when compared with the fentanyl plus droperidol anesthesia or sham-operated groups (P < 0.05). Inactivation of xanthine oxidase abrogated the alveolar-capillary membrane compromise associated with desflurane. Although significantly greater than for sham-operated animals, plasma xanthine oxidase activities released after aortic occlusion-reperfusion were not different between the two anesthetics. There were no anesthetic-associated differences in lung tissue xanthine oxidase activity. However, desflurane anesthesia resulted in a significant reduction in lung ascorbic acid after aortic occlusion-reperfusion compared with the sham-operated animals.